The general objectives of this research project are to show that: (1) increased concentrations of oxygen at normal atmospheric pressures induce biochemically measurable changes in newborn mouse lung in vivo, such as acute and chronic inhibition of DNA synthesis, (2) such changes directly relate to the increased oxygen concentration and duration of exposure (3) and that the injury induced by oxygen is manifested by damage to the cells of the bronchiolar mucosa and alveoli. This coming year we intend to (1) continue the characterization of short and long-term recovery from acute, subacute, and chronic exposure to 40, 60, 80 and 100% oxygen, (2) continue the identification autoradiographically of the major cellular regions involved in the spontaneous recovery from DNA syntesis inhibition, (3) begin identification of the specific cell types most sensitive to the acute inhibition of DNA synthesis, (4) and continue and expand the characterization of collagen deposition in the lung resulting from continuous exposure to 40, 60, 80 and 100% oxygen. BIBLIOGRAPHIC REFERENCES: Northway, W.H., Jr., Rezeau, L., Petriceks, R., Bensch, K.G.: Oxygen toxicity in the newborn lung: Reversal of inhibition of DNA synthesis in the mouse. Pediatrics, 57: 41-46, 1976. Bonikos, D.S., Bensch, K.G., Watt, T. and Northway, W.H., Jr.: Pulmonary oncocytes in prolonged hyperoxia. In Press. Experimental and Molecular Pathology, February, 1977.